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DPreclinical / mechanistic only
High riskNo human data

YK-11

YK-11 is a synthetic, steroidal (19-norprogesterone/norpregnadiene-derived) selective androgen receptor modulator (SARM) marketed to bodybuilders as a "myostatin inhibitor." Its reputation comes entirely from cell-culture and rodent experiments: it acts as a partial androgen-receptor agonist and drives muscle-cell differentiation by inducing follistatin (which antagonizes myostatin). There are no human clinical trials and no pharmacological human safety data. It is not an approved drug anywhere, is banned by WADA, and is frequently sold, often mislabeled or undisclosed, in unregulated "research chemical" supplements that are chemically unstable. Because YK-11 is androgenic and structurally closer to anabolic steroids than nonsteroidal SARMs, the class-wide human harms documented for SARMs apply and are the leading concern: serious cholestatic drug-induced liver injury (some cases requiring dialysis or causing bile-cast kidney injury), suppression of the body's own testosterone, and likely adverse cardiovascular/lipid effects. Rodent data additionally raise neurotoxicity concerns. Anyone using it should treat it as an unstudied androgen with real potential for organ injury.

Clinical readoutSARM · sarm-myostatin
Hepatic strainHigh
CardiovascularNone
HPTA suppressionNone
Half-life
Not established i…
Route
Oral
Evidence
D
Active
Unknown/not characteriz…
1·t½2·t½3·t½4·t½5·t½
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Not established in humans. The parent molecule is chemically unstable (orthoester D-ring moiety) and hydrolyzes within hours in vitro; intact YK-11 is generally not detectable in post-administration human urine.
Pharmacology

Mechanism of action

YK-11 binds the androgen receptor (AR) and acts as a partial/gene-selective agonist: it drives AR nuclear translocation and activates AR-target genes without inducing the normal amino/carboxyl-terminal (N/C) interaction, which underlies its "selective" transcriptional profile versus dihydrotestosterone (in vitro reporter assays). In C2C12 myoblasts it induces myogenic regulatory factors (MyoD, Myf5, myogenin) and, unlike DHT, up-regulates follistatin; follistatin antagonizes myostatin, so YK-11's "anti-myostatin" reputation is indirect (follistatin induction), not direct myostatin binding, and its anabolic effect is blocked by anti-follistatin antibody and by AR antagonists. It also activates non-genomic Akt signaling and promotes osteoblast and mesenchymal-stem-cell differentiation in vitro/rodent bone models, and molecular-docking work suggests inhibition of 5-alpha-reductase type II. All mechanism data are preclinical (cell lines and rodents).
Kinetics

Pharmacokinetics

Half-life

Not established in humans. The parent molecule is chemically unstable (orthoester D-ring moiety) and hydrolyzes within hours in vitro; intact YK-11 is generally not detectable in post-administration human urine.

Active duration

Unknown/not characterized in humans. In a human elimination study using deuterated YK-11, unconjugated metabolites cleared within ~24 hours while glucuronidated and sulfated metabolites remained detectable in urine for >48 hours (analytical detection window, not a measure of biological effect).

Route

Oral (the form found in illicit supplement products and used in reported administration studies).

Metabolism & clearance

Extensive hepatic metabolism to numerous phase I/II metabolites (O-demethylation, hydroxylation, then glucuronide and sulfate conjugation) with renal excretion of conjugated metabolites; parent compound is largely hydrolyzed/metabolized. Characterized only in human doping-control metabolism work and equine studies; reported for monitoring/washout context, not clinical dosing.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Preclinical (cell/rodent) anabolic signaling in skeletal muscle via AR activation and follistatin induction; promoted myoblast differentiation more strongly than DHT in vitro
  • Preclinical promotion of osteoblast proliferation/differentiation and bone-defect repair in rodents (bone-anabolic signal, in vitro and in vivo animal only)
  • Marketed to users for muscle hypertrophy, strength, and reduced body fat, but no human efficacy data exist to support these claims
  • Androgenic activity expected from AR agonism; magnitude and tissue selectivity in humans are unknown
  • Reported neuroactive effects in rodents (crosses into brain tissue in modeling) with adverse rather than beneficial CNS findings
Safety

Adverse effects by system

Cardiovascular

No YK-11-specific human data. As an androgenic AR agonist, adverse lipid changes (HDL suppression) and cardiovascular strain are mechanistically expected and are described among the class-level concerns for SARMs in human case literature. Treat cardiovascular risk as real but uncharacterized.

Hepatic

No YK-11-specific human case reports were identified, but drug-induced liver injury is the best-documented serious human harm of the SARM class. Multiple case reports/series and a systematic review describe cholestatic hepatocellular injury (including severe jaundice, bilirubin >30-40 mg/dL, cases requiring albumin dialysis, and one bile-cast nephropathy) after other SARMs (ostarine/enobosarm, RAD-140, LGD-4033, stenabolic). Because YK-11 is steroidal and structurally closer to anabolic steroids, it should be presumed to carry at least comparable hepatotoxic potential.

Endocrine / HPTA

No direct human data for YK-11. As an androgen-receptor agonist it is expected to suppress the hypothalamic-pituitary-testicular axis and lower endogenous testosterone, as documented for androgens and other SARMs; degree and reversibility in humans are unknown.

Reproductive

No YK-11-specific human data. Via HPTA suppression, androgenic SARMs can reduce spermatogenesis, testicular size, libido and fertility; these are expected but undocumented for YK-11 specifically.

Neuropsychiatric

No YK-11-specific human data. Psychiatric disturbances are listed among class-level SARM concerns in case literature; rodent YK-11 studies showed neuroinflammation and impaired aversive-memory consolidation, but human relevance is unknown.

Renal

No YK-11-specific data. Secondary acute kidney injury (bile-cast nephropathy) has been reported as a consequence of severe SARM-associated cholestatic liver injury; direct nephrotoxicity is not established.

Hematologic

No YK-11-specific data. Androgens can raise hematocrit/erythrocytosis; whether YK-11 does so in humans is unknown and unstudied.

Dermatologic

No YK-11-specific data. Androgenic dermatologic effects (acne, oily skin, potential hair changes) are plausible from AR agonism but unquantified in humans.

Recovery

HPTA suppression & recovery

Suppression: Expected but unquantified (no human data for YK-11)

YK-11 is an androgen-receptor agonist and, like other androgens/SARMs, is expected to suppress endogenous testosterone production; there are no human studies defining how much it suppresses the axis or how long recovery takes. Any suppression, and any decision about whether, when, or how to support recovery, should be evaluated and managed by an endocrinologist or qualified physician using baseline and follow-up bloodwork. This monograph does not endorse or describe any self-directed post-cycle or SERM protocol; recovery of the HPTA is a medical matter requiring individualized clinical supervision.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Liver function panel (ALT, AST, ALP, GGT, total and direct bilirubin) at baseline and periodicallyTotal testosterone, free testosterone, LH, FSH (HPTA status)Fasting lipid panel (HDL, LDL, total cholesterol, triglycerides)Complete blood count including hematocrit/hemoglobinRenal function (creatinine, eGFR), especially if liver enzymes or bilirubin rise

Cadence: Baseline before any use; follow-up within roughly 4-6 weeks and promptly if any symptoms arise; ongoing periodic checks under a clinician. Given severe cholestatic injury can appear within weeks in SARM case reports, do not wait for scheduled testing if warning signs develop.

Warning signs — seek care
  • Jaundice (yellowing of skin/eyes), dark urine, pale stools
  • Itching (pruritus), right-upper-quadrant or abdominal pain, nausea/vomiting
  • Unusual fatigue, malaise, or unexplained weight loss
  • Reduced urine output or swelling (possible kidney involvement)
  • Chest pain, palpitations, or breathlessness
  • Marked mood changes, depression, or aggression
  • Loss of libido, testicular shrinkage, or erectile dysfunction
Do not use if

Contraindications

  • Any pre-existing or prior liver disease, abnormal liver enzymes, or history of drug-induced liver injury
  • Pregnancy, breastfeeding, or possibility of pregnancy (androgenic; potential fetal harm)
  • Adolescents and anyone whose growth/HPTA is still developing
  • Existing cardiovascular disease, dyslipidemia, or significant cardiac risk factors
  • Personal or family history of hormone-sensitive cancer (e.g., prostate) given androgen-receptor agonism
  • Concurrent use of other hepatotoxic agents, anabolic-androgenic steroids, or other SARMs
  • Competitive/tested athletes (prohibited by WADA at all times)
  • Anyone unable or unwilling to obtain baseline and follow-up clinical monitoring
Combinations

Interaction profile

  • ModerateWith a thermogenic stimulant: Additive cardiovascular strain
  • MajorWith a 17α-alkylated oral: Additive liver strain
  • ModerateWith another liver-signal SARM: Additive liver strain
  • ModerateWith an anabolic steroid: Hormonal
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • There is no established safe dose: YK-11 has never been tested in a human clinical trial, and no human pharmacokinetic or safety dosing exists, so any dose is experimental.
  • Products sold as YK-11 are frequently mislabeled, unstable, or contain undisclosed SARMs; you often cannot know what or how much you are taking.
  • Stop immediately and seek urgent medical care for any sign of liver injury: jaundice, dark urine, pale stools, itching, right-upper-quadrant pain, nausea, or unusual fatigue. Severe cholestatic injury has appeared within weeks with related SARMs.
  • Get baseline bloodwork (liver panel, lipids, testosterone/LH/FSH, CBC) before use and follow-up testing, ideally under a physician; do not rely on feeling well, since liver and lipid changes can be silent.
  • Avoid combining with alcohol, other hepatotoxic drugs, anabolic steroids, or other SARMs, which compounds liver and cardiovascular risk.
  • Do not use if you have liver disease, cardiovascular disease, hormone-sensitive cancer risk, or if pregnant/breastfeeding, or if you are an adolescent.
  • HPTA suppression and recovery should be assessed and managed by an endocrinologist with bloodwork. Do not self-manage hormonal recovery.
  • The most conservative harm-reduction step is not to use YK-11; if used, involve a clinician and stop at the first abnormal lab or symptom.
Evidence

Citations (19)

Every clinical claim above is tied to a primary source. Overall evidence grade D — this compound lacks adequate human data; claims rest on preclinical or mechanistic evidence.

  1. 01

    YK-11 is a partial/gene-selective androgen-receptor agonist that activates AR and drives nuclear translocation without inducing the N/C interaction.

    Preclinical(17α,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester (YK11) is a partial agonist of the androgen receptor.PMID 21372378 ↗

  2. 02

    YK-11 induces myogenic differentiation of C2C12 myoblasts and up-regulates follistatin (which antagonizes myostatin); its anabolic effect depends on follistatin and AR.

    PreclinicalSelective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression.PMID 23995658 ↗

  3. 03

    YK-11 promotes osteoblast proliferation and differentiation in vitro via AR and non-genomic Akt signaling.

    PreclinicalSelective Androgen Receptor Modulator, YK11, Up-Regulates Osteoblastic Proliferation and Differentiation in MC3T3-E1 Cells.PMID 29491216 ↗

  4. 04

    YK-11 promotes osteogenic differentiation of bone-marrow mesenchymal stem cells and bone-defect repair in rats via AR activation.

    PreclinicalYK11 promotes osteogenic differentiation of BMSCs and repair of bone defects.PMID 39660819 ↗

  5. 05

    Gene-selective AR transactivation by YK-11 arises from differential DNA-binding and cofactor recruitment versus DHT.

    PreclinicalDifferential DNA-binding and cofactor recruitment are possible determinants of the synthetic steroid YK11-dependent gene expression by androgen receptor in breast cancer MDA-MB 453 cells.PMID 36030969 ↗

  6. 06

    YK-11 reduced muscle wasting and inflammation in a bacterial-sepsis mouse model (myostatin/follistatin pathway).

    PreclinicalMyostatin inhibitor YK11 as a preventative health supplement for bacterial sepsis.PMID 33588136 ↗

  7. 07

    YK-11 induced oxidative stress and mitochondrial dysfunction in the rat hippocampus (neurotoxicity signal).

    PreclinicalYK11 induces oxidative stress and mitochondrial dysfunction in hippocampus: The interplay between a selective androgen receptor modulator (SARM) and exercise.PMID 37468001 ↗

  8. 08

    YK-11 at anabolic doses altered hippocampal neurochemistry, increased pro-inflammatory cytokines, promoted apoptotic signaling, and impaired memory consolidation in rats; docking suggested 5-alpha-reductase II inhibition and brain permeability.

    PreclinicalFrom gains to gaps? How Selective Androgen Receptor Modulator (SARM) YK11 impact hippocampal function: In silico, in vivo, and ex vivo perspectives.PMID 38521455 ↗

  9. 09

    In a human deuterated-YK-11 elimination study, no intact parent was detected in urine; unconjugated metabolites cleared within ~24 h while glucuronidated/sulfated metabolites persisted >48 h.

    Case reportStudies on the in vivo metabolism of the SARM YK11: Identification and characterization of metabolites potentially useful for doping controls.PMID 30379415 ↗

  10. 10

    YK-11 is chemically unstable, hydrolyzing within hours, and has been detected—sometimes undisclosed—in unregulated dietary supplements.

    PreclinicalDevelopment and validation of liquid chromatography-tandem mass spectrometry method for screening six selective androgen receptor modulators in dietary supplements.PMID 33934684 ↗

  11. 11

    YK-11 undergoes extensive hepatic phase I/II metabolism (O-demethylation, hydroxylation, glucuronide/sulfate conjugation) with the parent largely hydrolyzed (equine in vivo model).

    PreclinicalEquine metabolism of the selective androgen receptor modulator YK-11 in urine and plasma following oral administration.PMID 36519889 ↗

  12. 12

    YK-11 use is detectable as a doping-control adverse analytical finding in humans and is prohibited in sport.

    Case reportDetection of selective androgen receptor modulator YK-11 in a doping control sample.PMID 37946705 ↗

  13. 13

    SARMs are prohibited by WADA and are misused for muscle/bone-anabolic effects despite none having full clinical approval; YK-11 is a steroidal SARM.

    ReviewDetection of SARMs in doping control analysis.PMID 28137616 ↗

  14. 14

    Systematic review of SARM safety in healthy adults documents drug-induced liver injury (15 case reports), tendon rupture, rhabdomyolysis, and ALT elevation (mean ~7.1% in trials); recreational SARM use should be strongly discouraged.

    ReviewSystematic Review of Safety of Selective Androgen Receptor Modulators in Healthy Adults: Implications for Recreational Users.PMID 37218811 ↗

  15. 15

    Ostarine (enobosarm) caused severe cholestatic liver injury with bilirubin >30 mg/dL requiring albumin dialysis in a healthy young man.

    Case reportLiver Injury after Selective Androgen Receptor Modulator Intake: A Case Report and Review of the Literature.PMID 37871633 ↗

  16. 16

    RAD-140 caused cholestatic drug-induced liver injury (peak bilirubin 38.5 mg/dL) confirmed on biopsy.

    Case reportRAD-140 Drug-Induced Liver Injury.PMID 36561105 ↗

  17. 17

    LGD-4033 (ligandrol) caused drug-induced liver injury with pruritic jaundice; SARMs are associated with hepatotoxicity, cardiovascular, endocrine, and psychiatric adverse effects.

    Case reportLGD-4033 and a Case of Drug-Induced Liver Injury: Exploring the Clinical Implications of Off-Label Selective Androgen Receptor Modulator Use in Healthy Adults.PMID 39421081 ↗

  18. 18

    Severe SARM-associated cholestatic liver injury caused secondary bile-cast nephropathy (acute kidney injury) requiring plasmapheresis.

    Case reportBile Cast Nephropathy Because of Acute Liver Injury Associated With Selective Androgen Receptor Modulators.PMID 37501938 ↗

  19. 19

    Stenabolic (SARM-marketed agent) was associated with hepatocellular drug-induced liver injury; SARM-class agents share hepatotoxic risk.

    Case reportWhen Gains Go Wrong: A Case of Selective Androgen Receptor Modulator-Related Liver Injury.PMID 40765588 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice